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Transferrin saturation and recovery from coma in cerebral malaria
V R Gordeuk1, P E Thuma, C E McLaren
1Department of Medicine, George Washington University Medical Center, Washington, DC 20037, USA.
Insights
Elevated transferrin saturation in severe malaria patients correlates with delayed recovery from cerebral malaria coma. Iron chelation therapy may improve outcomes in these cases.
Area of Science:
- Tropical Medicine
- Hematology
- Infectious Diseases
Background:
- Severe malaria, particularly cerebral malaria, can present with elevated transferrin saturations.
- The clinical significance of these elevated iron-related markers in malaria outcomes is not fully understood.
Purpose of the Study:
- To investigate the association between elevated transferrin saturation and adverse outcomes in children with cerebral malaria.
- To evaluate the potential benefit of iron chelation therapy in this patient group.
Main Methods:
- Retrospective analysis of serum samples from 81 Zambian children with cerebral malaria.
- Measurement of baseline transferrin saturations in patients treated with quinine and either placebo or desferrioxamine B.
- Comparison of time to recovery of consciousness based on transferrin saturation levels and treatment group.
Main Results:
- Over one-third of children exhibited transferrin saturations above 43%.
- Elevated transferrin saturation was linked to significantly delayed recovery from coma in the placebo group (68.2 vs. 25.4 hours).
- Iron chelation therapy appeared to accelerate recovery in children with high transferrin saturation.
Conclusions:
- Increased transferrin saturation may indicate a poorer prognosis and delayed recovery in cerebral malaria.
- Measuring serum iron and total iron-binding capacity is recommended for future malaria studies.
- Iron chelation warrants further investigation as an adjunctive therapy for severe malaria.
Abstract:
To determine if the elevated transferrin saturations found in some patients with severe malaria are associated with an adverse outcome in cerebral malaria, we retrospectively measured baseline saturations in stored serum samples from 81 Zambian children with strictly defined cerebral malaria. The children had been treated with quinine, sulfadox-ine-pyrimethamine, and intravenous infusions of either placebo (n = 39) or the iron chelator, desferrioxamine B (n = 42), in a previously reported trial (Gordeuk et al, N Engl J Med 327:1473, 1992). More than one-third of children in both the placebo- and iron chelator-treated groups had transferrin saturations exceeding 43%, which is 3 standard deviations above the expected mean for age. Among children receiving quinine and placebo, those with elevated transferrin saturations had a delayed estimated median time to recover full consciousness (68.2 hours) compared with those with saturations < or = 43% (25.4 hours; P = .006). The addition of iron chelation to quinine therapy in children with high saturations appeared to hasten recovery (P = .046). We conclude that increased transferrin saturations may be associated with delayed recovery from coma during standard therapy for cerebral malaria and that serum iron and total iron binding capacity should be measured in future studies.